1069-03-0Relevant articles and documents
Structural diversity of Burkholderia pseudomallei lipopolysaccharides affects innate immune signaling
Norris, Michael H.,Schweizer, Herbert P.,Tuanyok, Apichai
, (2017/05/12)
Burkholderia pseudomallei (Bp) causes the disease melioidosis. The main cause of mortality in this disease is septic shock triggered by the host responding to lipopolysaccharide (LPS) components of the Gram-negative outer membrane. Bp LPS is thought to be a weak inducer of the host immune system. LPS from several strains of Bp were purified and their ability to induce the inflammatory mediators TNF-α and iNOS in murine macrophages at low concentrations was investigated. Innate and adaptive immunity qPCR arrays were used to profile expression patterns of 84 gene targets in response to the different LPS types. Additional qPCR validation confirmed large differences in macrophage response. LPS from a high-virulence serotype B strain 576a and a virulent rough central nervous system tropic strain MSHR435 greatly induced the innate immune response indicating that the immunopathogenesis of these strains is different than in infections with strains similar to the prototype strain 1026b. The accumulation of autophagic vesicles was also increased in macrophages challenged with highly immunogenic Bp LPS. Gene induction and concomitant cytokine secretion profiles of human PBMCs in response to the various LPS were also investigated. MALDI-TOF/TOF was used to probe the lipid A portions of the LPS, indicating substantial structural differences that likely play a role in host response to LPS. These findings add to the evolving knowledge of host-response to bacterial LPS, which can be used to better understand septic shock in melioidosis patients and in the rational design of vaccines.
Synthesis and immunoreactivity of poly(acrylamide) copolymers containing C-3- and C-7-modified, carboxyl-reduced, 4-O- and 5-O-phosphorylated Kdo residues
Kosma,Strobl,Marz,Kusumoto,Fukase,Brade,Brade
, p. 93 - 107 (2007/10/02)
Sodium (allyl 3-deoxy-α-D-lyxo-2-heptulopyranosid)onate (6), allyl 3-deoxy-β- and -α-D-manno-2-octulopyranoside, sodium (allyl 3-deoxy-β-L-gulo-2-octulopyranosid)onate, sodium (allyl α-D-glycero-D-talo-2-octulopyranosid)onate, sodium (allyl α-D-glycero-D-galacto-2-octulopyranosidonate, ammonium (allyl 3-deoxy-4-O- and -5-O-phosphono-α-D-manno-2-octulopyranosid)onate, and ammonium (allyl 3-deoxy-4-O- and -5-O-phosphono-β-D-manno-2-octulopyranosid)onate were prepared and copolymerized with acrylamide to give multivalent haptens, which were used in immune inhibition assays. The monoclonal antibody A 20, directed against α-pyranoside Kdo residues, did not react with these compounds, except with heptulosonic acid derivative 6, thus proving that the terminal hydroxymethyl group of Kdo is not required for binding. Sodium (allyl 3-deoxy-α-D-(yxo-2-heptulopyranosid)onate (6), allyl 3-deoxy-β- and -α-D-manno-2-octulopyranoside, sodium (allyl 3-deoxy-β-L-gulo-2-octulopyranosid)onate, sodium (allyl α-D-glycero-D-talo-2-octulopyranosid)onate, sodium (allyl α-D-glycero-D-galacto-2-octolopyranosidonate, ammonium (allyl 3-deoxy-4-O- and -5-O-phosphono-α-D-manno-2-octulopyranosid)onate, and ammonium (allyl 3-deoxy-4-O- and -5-O-phosphono-β-D-manno-2-octulopyranosid)onate were prepared and copolymerized with acrylamide to give multivalent haptens, which were used in immune inhibition assays. The monoclonal antibody A 20, directed against α-pyranoside Kdo residues, did not react with these compounds, except with heptulosonic acid derivative 6, thus proving that the terminal hydroxymethyl group of Kdo is not required for binding.
